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Related Experiment Video

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Thyroid hormone dysfunction in MOGAD and other demyelinating diseases.

Ariel Rechtman1, Omri Zveik1, Nitsan Haham1

  • 1Department of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem. Jerusalem, Israel.

Journal of the Neurological Sciences
|January 19, 2024
PubMed
Summary

Thyroid hormones may influence central nervous system (CNS) demyelinating diseases like MOGAD. Higher FT3 in MOGAD and associations between TSH, FT4, and disease markers in NMOSD suggest potential therapeutic targets.

Keywords:
Brain volumeFT4MOGADNMOSDTSHThyroid hormones

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Area of Science:

  • Neuroimmunology
  • Endocrinology
  • Neurology

Background:

  • Thyroid hormones are crucial for neuronal and glial cell function.
  • Autoimmune thyroid diseases frequently co-occur with multiple sclerosis (MS).
  • Previous research suggests a link between thyroid hormones and neuromyelitis optica spectrum disorder (NMOSD), but not myelin oligodendrocyte glycoprotein-associated demyelination (MOGAD).

Purpose of the Study:

  • To investigate the role of thyroid hormones in CNS autoimmune demyelinating diseases.
  • To compare thyroid hormone levels in patients with MOGAD, NMOSD, MS, and other neurological disorders.
  • To explore correlations between thyroid hormone levels, disease severity (EDSS), and brain volume.

Main Methods:

  • Analyzed thyroid hormone levels (FT3, TSH, FT4) and clinical data (EDSS) in 26 MOGAD, 52 NMOSD, 167 MS, and 16 control patients.
  • Assessed volumetric brain information using magnetic resonance imaging (MRI) and the MDbrain platform.
  • Correlated hormone levels with Expanded Disability Status Scale (EDSS) scores and brain volumes.

Main Results:

  • MOGAD patients exhibited significantly higher free triiodothyronine (FT3) levels than NMOSD patients.
  • In NMOSD patients, elevated thyroid-stimulating hormone (TSH) correlated with lower disability and larger brain volume.
  • Higher free thyroxine (FT4) levels were observed in relapsing MOGAD and associated with increased disability and reduced brain volume in NMOSD.

Conclusions:

  • Thyroid hormone dysregulation may be involved in MOGAD and other CNS demyelinating disorders.
  • Specific thyroid hormone patterns differ between MOGAD and NMOSD, suggesting distinct pathophysiological roles.
  • Further research into thyroid axis mechanisms could reveal novel therapeutic strategies for demyelinating diseases.